Baylor College of Medicine co-hosted its annual “Update on Alzheimer’s Disease” on Nov. 8 in partnership with the Alzheimer’s Association Houston & Southeast Texas Chapter to share the latest in Alzheimer’s research with patients and caregivers, according to TMC News.
“This is really the center of our community as we gather and talk about various issues of the day,” Dan Baird, chair-elect of the Alzheimer’s Association Houston & Southeast Texas Chapter, said during the event. “We’re very pleased and it’s very fitting that this serves as a forum for Alzheimer’s disease and the progress that has been made.”
Alzheimer’s is a degenerative brain disease that affects memory and mental functions. According to the Alzheimer’s Association, Alzheimer’s is the sixth leading cause of death in the country, with one in three seniors dying with the disease or dementia. There are currently 5.7 million Americans living with Alzheimer’s and the number of patients is expected to increase to nearly 14 million by 2050.
Earlier this year, two peer-reviewed studies linking the herpes viruses to Alzheimer’s disease were published.
In one study, titled “Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus,” lead author Ben Readhead and his team found higher levels of human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) in subjects with Alzheimer’s compared to virus-free subjects and discovered that the presence of these viruses affect brain cells, leading to an accelerated progression of the disease.
The second study, titled “Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection,” found evidence that herpes virus in the brain may trigger the innate immune response to infection. The study showed that amino acids involved in Alzheimer’s disease progression, called beta-amyloid peptides, trap the herpes virus in the amyloid. Because the amyloids are in a sense protecting the brain by containing the virus, the brain automatically produces an army of amyloid to fight the virus. As a result, the build-up of amyloid between neurons disrupts cell communication and function.
Read the full story at TMC News.